Biochemistry
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Item Ethanol exacerbates manganese - induced functional alterations along the hypothalamic-pituitary-gonadal axis of male rats(Elsevier B.V., 2018) Nkpaaa, K. W.; Amadi, B. A.; Adedara, I. A; Wegwu, M. O.; Farombi, E. O.Manganese (Mn) exposure has been reported to induce reproductive dysfunction in animal and humans. Studies have shown that a large percentage of adolescent and adult populations tend to consume alcohol in a binge pattern. However, there is no information on the influence of alcohol on Mn - induced functional alteration along the hypothalamic - pituitary - gonadal axis. This study aimed to evaluate the influence of ethanol (EtOH) on Mn - induced functional alteration along the hypothalamic - pituitary - gonadal axis. Rats were exposed to Mn alone at 30 mg/kg body weight or co-expose with EtOH at 1.25 and 5 g/kg body weight for 35 consecutive days. Results showed that EtOH exposure significantly (p < 0.05) exacerbated Mn - induced decrease in anti- oxidant enzymes activities, glutathione level and increased oxidative stress biomarkers in the hypothalamus, testes an epididymis of the exposed rats. Moreover, induction of inflammation was associated with disruption of histo-architecture of the hypothalamus, testes and epididymis of rats treated with Mn alone, EtOH alone or in combination. Furthermore, EtOH significantly exacerbated Mn - induced diminution in reproductive hormones and marker enzymes of testicular functions coupled with decreased sperm quantity and quality. Taken together, EtOH exacerbates Mn - induced functional alteration along the hypothalamic - pituitary - gonadal axis in rats via mechanisms involving induction of oxidative/nitrosative stress, lipid peroxidation and inflammation in rats.Item Diphenyl diselenide abrogates brain oxidative injury and neurobehavioural deficits associated with pesticide chlorpyrifos exposure in rats(Elsevier B.V., 2018) Adedara, I. A. || || || || || ||; Owoeye, O.; Awogbindin, I. O.; Ajayi, O. B.; Adeyemo, O. A.; Rocha, J. B. T.; Farombi, E. O.Exposure to pesticide chlorpyrifos (CPF) is associated with neurodevelopmental toxicity both in humans and animals. Diphenyl diselenide (DPDS) is a simple synthetic organoselenium well reported to possess antioxidant, anti-inflammatory and neuroprotective effects. However, there is paucity of information on the beneficial effects of DPDS on CPF-mediated brain injury and neurobehavioural deficits. The present study investigated the neuroprotective mechanism of DPDSin rats sub-chronically treated with CPF alone at 5 mg/kg body weight or orally co-treated with DPDS at 2.5 and 5 mg/kg body weight for 35 consecutive days. Endpoint analyses using video- tracking software in a novel environment revealed that co-treatment with DPDS significantly (p < 0.05) pro- tected against CPF-mediated locomotor and motor deficits precisely the decrease in maximum speed, total distance travelled, body rotation, absolute turn angle, forelimb grip strength as well as the increase in negative geotaxis and incidence of fecal pellets. The enhancement in the neurobehavioral activities of rats co-treated with DPDS was verified by track plot analyses. Besides, DPDS assuaged CPF-induced decrease in acetylcholinesterase and antioxidant enzymes activities and the increase in myeloperoxidase activity and lipid peroxidation level in the mid-brain, cerebral cortex and cerebellum of the rats. Histologically, DPDS co-treatment abrogated CPF- mediated neuronal degeneration in the cerebral cortex, dentate gyrus and cornu ammonis3 in the treated rats. In conclusion, the neuroprotective mechanisms of DPDS is related to the prevention of oxidative stress, enhance- ment of redox status and acetylcholinesterase activity in brain regions of the rats. DPDS may be a promising chemotherapeutic agent against brain injury resulting from CPF exposure.Item Neuroprotective influence of taurine on fluoride-induced biochemical and behavioral deficits in rats(Elsevier Ireland Ltd., 2017) Adedara, I. A.; Abolaji, A. O.; Idris, U. F.; Olabiyi, B. F.; Onibiyo, E. M.; Ojuade, T. D.; Farombi, E. O.Epidemiological and experimental studies have demonstrated that excessive exposure to fluoride induced neurodevelopmental toxicity both in humans and animals. Taurine is a free intracellular b- amino acid with antioxidant and neuroprotective properties. The present study investigated the neu- roprotective mechanism of taurine by evaluating the biochemical and behavioral characteristics in rats exposed to sodium fluoride (NaF) singly in drinking water at 15 mg/L alone or orally co-administered by gavage with taurine at 100 and 200 mg/kg body weight for 45 consecutive days. Locomotor behavior was assessed using video-tracking software during a 10-min trial in a novel environment while the brain structures namely the hypothalamus, cerebrum and cerebellum of the rats were processed for biochemical determinations. Results showed that taurine administration prevented NaF-induced loco- motor and motor deficits namely decrease in total distance travelled, total body rotation, maximum speed, absolute turn angle along with weak forelimb grip, increased incidence of fecal pellets and time of grooming, immobility and negative geotaxis. The taurine mediated enhancement of the exploratory profiles of NaF-exposed rats was supported by track and occupancy plot analyses. Moreover, taurine prevented NaF-induced increase in hydrogen peroxide and lipid peroxidation levels but increased acetylcholinesterase and the antioxidant enzymes activities in the hypothalamus, cerebrum and cere- bellum of the rats. Collectively, taurine protected against NaF-induced neurotoxicity via mechanisms involving the restoration of acetylcholinesterase activity and antioxidant status with concomitant inhi- bition of lipid peroxidation in the brain of rats.Item Suppression of the brain-pituitary-testicular axis function following acute arsenic and manganese co-exposure and withdrawal in rats(Elsevier GmbH., 2017) Adedara, I. A.; Abolaji, A. O.; Awogbindin, I. O.; Farombi, E. O.Despite the fact that most environmental exposures to metals do not occur in isolation, the combined effects of metal mixtures on brain–pituitary–gonadal axis are poorly known. The present study investigated the impacts of co-exposure to arsenic (As) and manganese (Mn) on sperm characteristics, reproductive hormones and selected oxidative stress indices in the brain, testes and epididymis of rats following exposure for 15 consecutive days to 60 mg/L of AsO₃Na and 30 mg/L of MnCl₂ in drinking water. The results showed that while brain weight remained unaffected, the fluid intake and the weights of testes and epididymis significantly (p < 0.05) decreased in all the treatment groups. A significant decrease in the body weight gain when compared with control was noted only in the co-exposed rats. Moreover, the significant decreases in the antioxidant status in brain, testes and epididymis as well as in the circulatory concentrations of follicle-stimulating hormone, luteinizing hormone and testosterone were similar following separate or combined exposure of rats to As and Mn. The marked oxidative damage in the investigated tissues was accompanied by a significant decrease in the sperm quantity and quality in all the treated rats when compared with the control. Interestingly, most of the parameters determined immediately after the exposure period persisted in rats from the withdrawal experiment. Collectively, co-exposure to As and Mn suppressed the brain–pituitary–testicular axis function and the post-testicular events such as sperm function possibly via a mechanism involving persistent oxidative stress and endocrine disruption in the exposed rats.Item Quercetin improves neurobehavioral performance through restoration of brain antioxidant status and Acetylcholinesterase activity in Manganese-treated rats(Springer Science+Business Media, 2017) Adedara, I. A.; Ego, V. C.; Subair, T. I.; Oyediran, O.; Farombi, E. O.The present study investigated the neuroprotective mechanism of quercetin by assessing the biochemical and behavioral characteristics in rats sub-chronically treated with manganese alone at 15 mg/kg body weight or orally co-treated with quercetin at 10 and 20 mg/kg body weight for 45 consecutive days. Locomotor behavior was monitored using video-tracking software during a 10-min trial in a novel environment whereas the brain regions namely the hypothalamus, cerebrum and cerebellum of the rats were processed for biochemical analyses. Results indicated that co-treatment with quercetin significantly (p < 0.05) prevented manganese-induced locomotor and motor deficits specifically the decrease in total distance travelled, total body rotation, maximum speed, absolute turn angle as well as the increase in time of immobility and grooming. The improvement in the neurobehavioral performance of manganese-treated rats following quercetin co-treatment was confirmed by track and occupancy plot analyses. Moreover, quercetin assuaged manganese-induced decrease in antioxidant enzymes activities and the increase in acetylcholinesterase activity, hydrogen peroxide generation and lipid peroxidation levels in the hypothalamus, cerebrum and cerebellum of the rats. Taken together, quercetin mechanisms of ameliorating manganese-induced neurotoxicity is associated with restoration of acetylcholinesterase activity, augmentation of redox status and inhibition of lipid peroxidation in brain of rats.Item Benzo(a)pyrene induces oxidative stress, pro-inflammatory cytokines, expression of nuclear factor-kappa B and deregulation of wnt/beta- catenin signaling in colons of BALB/c mice201(Elsevier Ltd., 2016) Ajayi, B. O.; Adedara, I. A.; Farombi, E. O.The incidence of colonic toxicity has been epidemiologically linked to the consumption of foods contaminated with benzo[a]pyrene (B[a]P). The present study investigated the effects of B[a]P on biomarkers of colonic stress, inflammation and Wnt/β-catenin signaling in colon of BALB/c mice. B[a]P was administered orally at 62.5, 125 and 250 mg/kg of B[a]P for 7 days by oral gavage. Exposure to B[a]P significantly decreased the colonic antioxidant enzyme activities and glutathione levels with concomitant significant increase in myeloperoxidase activity, nitric oxide and lipid peroxidation levels. Colon histopathology results showed treatment-related lesions characterized by atrophy, mucosal ulceration and gland erosion in the B[a]P-treated mice. Immunohistochemistry analysis showed that B[a]P treatment increased the protein expression of nuclear factor kappa B, pro-inflammatory cytokines namely tumor necrosis factor alpha and interleukin-1β, as well as cyclooxygenase-2 and inducible nitric oxide synthase in the mice colon. Altered canonical Wnt signaling was confirmed using diaminobenzidine staining for p38 mitogen activated protein kinase, β-catenin expression and absence of adenomatous polyposis coli following B[a]P administration. The present data highlight that exposure to B[a]P induces colonic injury via induction of oxidative and nitrosative stress, inflammatory biomarkers and dysregulation of Wnt/β-catenin signaling, thus confirming the role of B[a]P in the pathogenesis of colonic toxicity.Item Dietary protocatechuic acid ameliorates dextran sulphate sodium-induced ulcerative colitis and hepatotoxicity in rats(The Royal Society of Chemistiy, 2016) Farombi, E. O. || || || || || || ||; Adedara, I. A.; Awoyemi, O. V.; Njoku, C. R.; Micah, G. O.; Esogwa, C. U.; Owumi, S. E.; Olopade, J. O.The present study investigated the antioxidant and anti-inflammatory effects of dietary protocatechuic acid (PCA), a simple hydrophilic phenolic compound commonly found in many edible vegetables, on dextran sulphate sodium (DSS)-induced ulcerative colitis and its associated hepatotoxicity in rats. PCA was administered orally at 10 mg kg-1 to dextran sulphate sodium exposed rats for five days. The result revealed that administration of PCA significantly (p < 0.05) prevented the incidence of diarrhea and bleed- ing, the decrease in the body weight gain, shortening of colon length and the increase in colon mass index in DSS-treated rats. Furthermore, PCA prevented the increase in the plasma levels of pro-inflamma- tory cytokines, markers of liver toxicity and markedly suppressed the DSS-mediated elevation in colonie nitric oxide concentration and myeloperoxidase activity in the treated rats. Administration of PCA significantly protected against colonie and hepatic oxidative damage by increasing the antioxidant status and concomitantly decreased hydrogen peroxide and lipid peroxidation levels in the DSS-treated rats. More- over, histological examinations confirmed PCA chemoprotection against colon and liver damage. Immunohistochemical analysis showed that PCA significantly inhibited cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) protein expression in the colon of DSS-treated rats. In conclusion, the effective chemoprotective role of PCA in colitis and the associated hepatotoxicity is related to its intrinsic anti-inflammatory and anti-oxidative properties.Item Redox status of the testes and sperm of rats following exposure to 2,5-hexanedione(Taylor & Francis Group, 2016) Adedara, I. A. || || || || ||; Abolaji, A. O.; Odion, B. E.; Omoloja, A. A.; Okwudi, I. J.; Farombi, E. O.Objectives: Exposure to 2, 5-hexanedione (2, 5-HD) is well known to be associated with reproductive dysfunctions in both humans and animals. However, the role of oxidative stress in 2, 5-HD-induced toxicity in testes and sperm has not yet been studied. Methodology: The present study investigated the influence of 2, 5-HD on antioxidant systems in the testes and epididymal sperm of rats following exposure to 0, 0.25, 0.5, and 1% 2, 5-HD in drinking water for 21 consecutive days. Results: Administration of 0.5% 2, 5-HD significantly (P < 0.05) decreased epididymis weight, whereas 1% 2, 5-HD-treated rats showed significantly decreased body weight, testis, and epididymis weights compared with the control group. Exposure to 2, 5-HD caused a significant dose-dependent increase in the activities of superoxide dismutase, catalase, and glutathione peroxidase in both testes and sperm compared with the control group. Moreover, 2, 5-HD-exposed rats showed significant decrease in glutathione-S-transferase activity and glutathione level with concomitant significant elevation in the levels of hydrogen peroxide and malondialdehyde in both testes and sperm. Testicular and epididymal atrophy with significant, dose-dependent, decrease in epididymal sperm number, sperm motility, and viability were observed in 2, 5-HD-treated rats. Conclusion: 2,5-HD exposure impaired testicular function and sperm characteristics by disruption of the antioxidant systems and consequently, increased oxidative stress in the treated rats.Item Neurobehavioral and biochemical changes in Nauphoeta cinerea following dietary exposure to chlorpyrifos(Elsevier Inc., 2016) Adedara, I. A.; Rosemberg, D. B.; Souza, D.; Farombi, E. O.; Aschner, M.; Souza, D. O.; Rocha, J. B. T.The present study aimed to increase our understanding about the mode of toxic action of organophosphate pesticides in insects by evaluating the biochemical and neurobehavioral characteristics in Nauphoeta cinerea exposed to chlorpyrifos (CPF)-contaminated diet. The insects were exposed for 35 consecutive days to CPF at 0.078, 0.15625, 0.3125 and 0.625 μg/g feed. Locomotor behavior was assessed for a 10-min trial in a novel arena and subsequently, biochemical analyses were carried out using the cockroaches’ heads. In comparison to control, CPF-exposed cockroaches showed significant decreases in the total distance traveled, body rotation, turn angle and meandering, along with significant increase in the number of falls, time and episodes of immobility. The marked decrease in the exploratory profiles of CPF-exposed cockroaches was confirmed by track plots, whereas occupancy plot analyses showed a progressive dispersion at 0.15625 μg/g feed group. Moreover, the heads of CPF-exposed cockroaches showed marked decrease in acetylcholinesterase activity and antioxidant status with concomitant significant elevation in dichlorofluorescein oxidation and lipid peroxidation levels in CPF-treated cockroaches. Gas Chromatography–Mass Spectrometry analyses revealed bioaccumulation of CPF in cockroaches exposed to concentrations above 0.078 μg/g feed. The findings from this investigation showed N. cinerea as a value model organism for the risk assessment of environmental organophosphate contamination in insects.Item Influence of diphenyl diselenide on chlorpyrifos-induced toxicity in Drosophila melanogaster(Elsevier GmbH., 2015) Adedara, I. A.; Klimaczewski, C. V.; Barbosa, N. B. V.; Farombi, E. O.; Souza, D. O.; Rocha, J. B. T.Exposure to chlorpyrifos (CPF) poses several harmful effects to human and animal health. The present study investigated the influence of diphenyl diselenide (DPDS) on CPF-induced toxicity in Drosophila melanogaster. Firstly, the cumulative responses of virgin flies (2- to 3-day-old) to CPF (0.075–0.6 µg/g) and DPDP (5–40 µmol/kg) in the diet for 28 consecutive days were investigated. Subsequently, the protective effect of DPDS (10, 20 and 40 µmol/kg) on CPF (0.15 µg/g)-induced mortality, locomotor deficits, neurotoxicity and oxidative stress was assessed in a co-exposure paradigm for 7 days. Results showed that CPF exposure significantly decreased the operant reflex in a time- and concentration-dependent manner, whereas the percent live flies with DPDS treatment was not statistically different from control following 28 days of treatment. In the co-exposure study, CPF significantly increased mortality while the survivors exhibited significant locomotor deficits with decreased acetylcholinesterase (AChE) activity. Dietary supplementation with DPDS was associated with marked decrease in mortality, improvement in locomotor activity and restoration of AChE activity in CPF-exposed flies. Moreover, CPF exposure significantly decreased catalase and glutathione-S-transferase activities, total thiol level with concomitant significant elevation in levels of reactive oxygen species and thiobarbituric acid reactive substances in the head and body regions of the treated flies. Dietary supplementation with DPDS significantly improved the antioxidant status and prevented CPF-induced oxidative stress, thus demonstrating the protective effect of DPDS in CPF-treated flies.